A 55-year-old woman on furosemide and omeprazole has persistent serum K+ of 2.8 mEq/L despite aggressive oral and intravenous potassium replacement for five days. Serum magnesium is 1.1 mg/dL. The most likely reason for refractory hypokalaemia is:

• A Reduced gastrointestinal absorption of oral potassium supplements
• B Insulin-mediated transcellular shift of administered potassium
• C Increased aldosterone independent of the renin-angiotensin axis
• D Disinhibited ROMK channels in the collecting duct allowing continued K+ secretion ✓

Explanation

Intracellular magnesium blocks ROMK channels in principal cells, limiting kaliuresis. When hypomagnesaemia coexists with diuretic-induced hypokalaemia, this brake is removed and secreted potassium escapes into urine regardless of replacement, producing refractory hypokalaemia. Correction of magnesium is required before serum potassium can be restored. Transcellular shift, autonomous aldosterone excess and malabsorption do not explain the combination of diuretic use, low magnesium and treatment resistance seen here.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.